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GI Flashcards

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1
Q

What happens when there’s a shift in the bidrectional flux in the small bowel?

A

Can result in overload of colonic absorptive capacity, leading to diarrhea

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2
Q

How do infections change the normal physio of the intestines?

A

Penetration through intact mucosa
Inflammatory or cytotoxic destruction of ileal/colonic mucosa
Shift in bidrectional water and electrolyte flow in upper small intestine

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3
Q

Ex of penetration through intact mucosa–organisms

A

Listeria

Salmonella typhi

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4
Q

Ex of inflammation or cytotoxic destruction of ileal or colonic mucosa

A 
Shigella
Non typhoidal salmonella types
enterohermoorhagic e coli
campylobacter
helicobacter
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5
Q

ex of shift in bidirectional water and electrolyte flow–name organism

A

vibrio cholerae

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6
Q

listeria metabolism, spore/no spore, stain and shape

A

aerobic
no spores
gram positive
rod

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7
Q

What is unique about Listeria?

A

grows at 1-45 C and high salt (think stored foods!)

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8
Q

motility/non-motility of listeria?

A

motile at room temp

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9
Q

What helps to ID listeria microscopically?

A

Tumbling

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10
Q

Who does Listeria cause disease in?

A

neonates, elderly, pregnant, immunocompromised

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11
Q

Pathogenesis of Listeria

A

consume contaminated food
L. monocytogenes survives in acid and bile salts
adheres to host cell
enters enterocytes or M cells
pH in phagosome induces listeriolysin O and 2 phospholipase C enzymes
Listeria replicates freely in cytoplasm
ActA on Listeria polymerizes host actin and enables it to move intracellularly to membrane
Actin polymerization

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12
Q

What kind of symptoms do you see for Listeria in the healthy?

A

mild flu like
acute
self limited gastroenteritis

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13
Q

What kind of symptoms do you see for Listeria in the immunocrompromised adult?

A

meningitis, high mortality

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14
Q

symptoms of listeria in neonate?

A

early onset-abortion, stillbirth, premature birth
granuloma formation in many organs
late onset-meningitis

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15
Q

Stain and shape of Salmonella

A

gram negative

rod

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16
Q

Where are salmonella found

A

soil, water, normal intestinal flora

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17
Q

Does Salmonella ferment or not ferment lactose?

A

does not

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18
Q

Pathogenesis of Salmonella

A

withstands stomach acid
attaches to small intestine and invades M cells and enterocytes
Replicates in endocytic vacuoles
endocytic vacules are stabilized by injection of Salmonella proteins with two type III secretion systems

Type III secretion systems (pathogenicity island 1=injected into host cell to tell cell to take up Salmonella) (pathogenicity island 2=injected into cytoplasm of host cell to resist phago-lysosome fusion)

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19
Q

Salmonella can cause

A

Gastroenteritis (serotypes other than Typhi and paratyphi)
enteric or typhoid fever (for typhi, bacteria not only invade enterocytes but replicates in macrophages–spreads through reiculoentheolial system to liver, spleen, blood)

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20
Q

Salmonella causes gastroenteritis commonly in?

A

children and elderly, more frequent in summer

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21
Q

Where is Salmonella found?

A

food (poultry, eggs, ground beef)

pet turtle feces

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22
Q

Differences between salmonella typhi and salmonella causing gastroenteritis?

A

inoculum is low for typhi

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23
Q

How does one get Salmonella typhi?

A

person to person, fecal contamination

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24
Q

Which has a vaccine? Listeria or Salmonella

A

Salmonella (use for travel)

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25
diseases of Salmonella
``` gastroenteritis (fever, abd cramps, headache, nonbloody diarrhea) salmonella septicemia (can be caused by all species) enteric fever-(colonizes gall bladder and reinfects intestines) ```
26
Salmonella is lactose positive or negative?
lactose negative
27
Salmonella is motile or non motile?
motile
28
What chemical does Salmonella make?
H2S
29
stain, motility, metabolism of shigella
gram negative non motile does not ferment lactose
30
Does shigella have or not have a capsule?
no capsule
31
How is Shigella spread?
fecal oral
32
Pathogenesis of shigella
replicate intracellulary in COLON invade M cells initially in small intestine inject type III proteins into host cells to be engulfed (proteins are IpaA, IpaB, IpaC, IpaD) inside cells, shigella lyses the vacuole and replicates freely in cytoplasm polymerizes host actin to move to other cells induce apoptosis of phagocytic cells make Shiga toxin
33
How does Shiga toxin work?
enzymatic A component cleaves 28S ribosomal RNA--causes colon's epithelium to die
34
Who does Shigella cause disease in?
mostly children
35
symptoms of shigella
``` abdominal cramps tenesmus (strain to defecate) diarrhea pus and blood in stool neutrophils and mucous in stool dysentery (frequent stool w blood and mucous-cells sloughed off) ```
36
What do Shigella appear like in culture?
lactose negative on selective medium (colorless colony on MacConkey agar)
37
Differences btwn Shigella and Salmonella? Similarities?
both are lactose negative shigella is non motile, salmonella has flagella shigella doesn't make H2S
38
How do you treat Shigella?
mild infections are self limiting | antibiotics only given for serious cases
39
Why is giving an antidiarrheal drug not good for Shigella
can make toxin stay longer in host instead of allowing it to be flushed out--causes more cell death
40
What are the Enterobacteriaceae in gram stain?
negative
41
How is enterohemorrhagic E. coli spread?
fecal oral
42
Is Enterohemorrhagic E coli an opportunistic pathogen or true pathogen?
true pathogen
43
What do EHEC produce that is cytotoxic?
Shiga toxin
44
EHEC pathogenesis
makes a type III secretion system to enable it to be ingested by host cell Also injects Tir, which binds to EHEC's OM protein intimin EHEC grows in place and produces Shiga toxin
45
How are Shiga toxin genes in EHEC?
Bacteriophage
46
How does one get EHEC?
consume undercooked beef, meat, anything contaminated with cattle feces
47
Disease symptoms of EHEC?
ranges from mild diarrhea to hemorrhagic colitis
48
What is hemorrhagic colitis?
intense abdominal pain and bloody diarrhea happening 3-4 days after eating food contaminated with EHEC
49
In children, what can EHEC cause?
hemolytic uremic syndrome (acute renal failure, hemolytic anemia)
50
How to differentiate EHEC in culture?
unable to ferment sorbitol--differential sorbitol containing MacConkey agar on which E coli are pink but EHEC is colorless
51
Treatment for EHEC?
not given antibiotics --(in experiments antibiotics increased Shiga toxin release) monitor in case develop microangiopathic complications (HUS)
52
Stain, shape, metabolism, motility of Campylobacter
gram negative curved rod (spiral or comma) non-fermentative (microaerophilic) motile with single flagella at one or two poles
53
What temp can Campylobacter grow?
42
54
Pathogenesis of Campylobacter
inflammation of small intestine and colon, diarrhea Ulcers infections linked with autoimmune disorders (guillain barre, reactive arthritis)---so due to LPS and cross reactivity Makes toxin that stops cell division
55
How do you get campylobacter?
consume contaminated food (especially chicken)
56
When are Campylobacter infections most abundant?
summer and early fall
57
Symptoms of Campylobacter infection
diarrhea (MORE THAN 10 bowel mvmts/day) bloody stool fever abd pain, inflammation, ulcer
58
Microscopy of Campylobacter
darting motility S shaped in stool RBCs and WBCs in stool
59
Culture of Campylobacter
difficult--slowly grows, microaerophile, higher temps
60
Treatment of Campylobacter
``` fluid replacement (for diarrhea) Serious cases-give antibiotics ```
61
Stain, shape, motility, metabolism of Helicobacter
gram negative curved rod multiple flagella microaerophilic
62
What enzyme in helicobacter converts urea to NH3 and CO2?
urease
63
Culture of Helicobacter
difficult. also difficult to isolate
64
How does urease help Helicobacter?
helps it survive in acidic conditions of stomach
65
Survivial mechanisms of Helicobacter in stomach
urease for acid swim through mucus with flagella stick to gastric epithelium (lewis blood group Ags and laminin) pH at epithelial surface = 7
66
Pathogenesis of Helicobacter
2 LOCI: Toxin VacA--makes an anion specific channel, forms large vacuoles in cells, changes tight jxns, causes gastric epithelial erosion SECOND locus: multiple genes (type IV secretion system that injects CagA inducing IL-8 release, enhance IL-8 transcription, Type IV effectos that cause pedestal formation)
67
Symptoms of Helicobacter infection
gastritis gastric ulcer formation but asymptomatic in 70-80% of infected
68
Transmission of Helicobacter
fecal oral
69
Diagnosis of Helicobacter
urea breath test (labeled urea) histology of gastric biopsy biochemical detect. urease in gastric biopsy h pylori antigens from stool samples
70
Stain, shape of vibrio, motility
gram negative curved rod single polar flagella
71
Pathogenesis of Vibrio
Cholera toxin. Cholera toxin is encoded by bacteriophage Toxin binds to ganglioside receptor on intestinal epithelial cells A subunit ADP ribsylates Gs--increased cAMP---stimulates CFTR causing Cl- secretion, inhibts NaCL absoprtion, results in net water loss OSMOTIC DIARRHEA Also encoded from phage: TCP-toxin coregulated pilus for attachment chemotaxis proteins to get vibrio to host epithelial cells
72
How does vibrio still produce diarrhea without cholera toxin?
zonnula occludens toxin--disrupts tight jxns | accessory cholera enterotoxin--increases fluid secretion
73
Where are Vibrio found?
marine environments
74
How is cholera spread to humans?
contaminated water and food (asymptomatic individuals can shed organism) NO human to human transmission b/c high infectious dose needed

Bacteria (6 decks)

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